Case Presentation: The patient is a 41-year-old female with history of iron deficiency anemia previously on IV iron transfusions and menorrhagia status post myomectomy presented to the emergency department with complaints of new-onset petechiae, spontaneous bruising, and gingival bleeding. The patient reported that in the duration of 2 days, she developed in bruising throughout her body, ranging from her arms and legs and including her mucosal surfaces her mouth. Eight months prior to presentation, she had initiated weekly compounded Tirzepatide (dose escalated to 10 mg/week over 6 weeks) obtained from a local compounding pharmacy as part of a non-physician-supervised weight management program. She reported no other new medications, herbal supplements, or over-the-counter agents. She could not isolate any other deviance to her daily life. On examination, she was noted to have multiple areas of non-blanching petechiae throughout the abdomen, lower extremities, upper extremities, and facial areas with areas of ecchymosis on her lower extremities. On oral examination, there was a small area of purpura with a background of multiple areas of petechiae. No lymphadenopathy or hepatosplenomegaly was present. Laboratory evaluation showed platelet count < 2,000/µL with peripheral blood smear showing marked thrombocytopenia with large platelets and no schistocytes. Coagulation panel showed a PT/INR and aPTT within reference range. Given the temporal association with compounded Tirzepatide, absence of other triggers, and lack of systemic symptoms, drug-induced immune thrombocytopenic purpura (ITP) was strongly suspected. The medication was immediately discontinued. The patient received intravenous immunoglobulin (IVIG) at 1 g/kg for 2 consecutive days along with IV Solumedrol. She was then transitioned to oral prednisone (60 mg/day). Over the following week, her platelet counts increased, reaching 148,000/µL by day 4 and normalizing (>150,000/µL) by day 5. No further bleeding events occurred, and corticosteroids were slowly tapered over the next month.The patient remains in clinical remission six months after cessation of Tirzepatide, with no recurrent thrombocytopenia.
Discussion: Drug induced immune thrombocytopenic purpura (ITP) is characterized by autoimmune destruction of platelets, via hapten formation or autoantibody generation against platelet antigens, that can present weeks to months of exposure to a causative agent. Tirzepatide, a dual GIP and GLP-1 receptor agonist, has rapidly gained popularity due to its efficacy in weight reduction and glycemic control; however, compounded forms lack quality control safeguards of commercial preparations, potentially introducing immunogenic contaminants. Given the potential for immunogenic reactions and variability in compounding practices, clinicians should exercise caution in patients utilizing non-commercial medications. Furthermore, the pathophysiology in this context should be explored to establish guidelines for safe prescribing and potentially surveillance.
Conclusions: While Tirzepatide has very rare reports of hematological adverse events, novel excipients or altered protein structure in compounded Tirzepatide may trigger an immune response. Clinicians should maintain a high index of suspicion for ITP in patients presenting with unexplained thrombocytopenia and bleeding symptoms in the context of recent exposure to compounded medications.